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Alcoholic Cardiomyopathy: Overview, Cardiac Effects of Alcohol, Quantity of Alcohol Intake in Cardiac Disease

cardiomyopathy alcohol

Specifically, ethanol disturbs the ryanodine Ca2+ release, the sarcomere Ca2+sensitivity 102,103, the excitation–contraction coupling and myofibrillary structure, and protein expression, decreasing heart contraction 86. Ethanol-induced disruption of ribosomal protein synthesis also contributes to non-contractile protein depletion 104. Several aspects of mitochondrial function, including respiratory complex activities and mitochondrial-dependent oxidative damage and apoptosis, are also induced by ethanol 26,100.

  • In addition, it provides information not only on overall heart size and function, but on valvular structure and function, wall motion and thickness, and pericardial disease.
  • Ethanol-induced changes may be related to oxidative or nonoxidative pathways of ethanol metabolism.
  • In CAD, diabetes, and stroke prevention the J‑type mortality curves even indicate some benefit apart from the social ”well-being“.
  • Unfortunately, all the available reports were completed at a time when a majority of the current heart failure therapies were not available (Table 1).

Alcoholic cardiomyopathy

cardiomyopathy alcohol

Alcohol septal ablation is a good alternative for people who can’t have open-heart surgery. Due to page limitations, we recognize that we have not included all the excellent scientific work completed in the area of alcohol and the cardiovascular system. Moreover, ranolazine prevents ethanol-induced atrial arrhythmias both in vitro and in vivo by blocking the late sodium current, which is activated by CaMKII.112 Its effect on preventing the decrease of LVEF in AC is currently unknown. This review will provide an updated view of this condition, including its epidemiology, pathogenesis, diagnosis, and treatment (Graphical Abstract). Around 40–80% of people with ACM who continue drinking alcohol die within 10 years of their diagnosis.

Treatment

cardiomyopathy alcohol

Finally, we analyzed and presented the synthesized literature, along with relevant findings and conclusions from the included studies, in a coherent manner. We identified main themes and sub-themes to provide a comprehensive overview of the current state of knowledge regarding ACM. By following this methodology, we aim to contribute to the existing body of knowledge on ACM, providing a reliable and up-to-date understanding of its pathogenesis, clinical features, diagnostic approaches, treatment options, and potential preventive strategies.

cardiomyopathy alcohol

What is alcoholic cardiomyopathy?

However, ascertaining the exact alcohol consumption threshold for determining both the benefit and risk has been challenging, and threshold levels continue to differ across studies. New strategies to improve the natural course of ACM have been proposed as promising agents in this field 112,147. Since ethanol has multiple cell targets with different pathological mechanisms implicated, those different strategies to cardiomyopathy alcohol directly target alcohol-induced heart damage are only partially effective and can only be used as support medication in a multidisciplinary approach 112.

  • On ECG, unspecific abnormalities like complete or incomplete left bundle branch block, atrioventricular conduction disturbances, alterations in the ST segment, and P wave changes can be found comparable to those in idiopathic DCM 113.
  • Note that the heart walls are much thicker in the heart with hypertrophic cardiomyopathy.
  • Others have examined the potential effects of micronutrient deficiencies (such as zinc) on ethanol-induced changes in the heart.
  • Others have demonstrated that long-term ethanol administration decreases myocardial protein expression and synthesis and accelerates protein degradation, suggesting that these alterations may represent a key pathophysiologic mechanism underlying the adverse effects of ethanol (62).

Acute vs. chronic

Summary of studies using pharmacologic inhibition or genetic manipulation to suppress ethanol-induced changes in cardiac structure and function. A case of rapid reversal of alcohol-induced cardiomyopathy with abstinence is reviewed. The present case highlights the acute toxic nature of alcohol and the potential for rapid functional recovery. Furthermore, alcohol consumption has also been classified in the literature by ranges of consumption as mild, moderate, and heavy drinking.11 In this regard, these categories have the following consumption thresholds that also differ according to sex. Elevations in troponin can signify heart damage or an increase in cardiac output that results in demand ischemia.